Fusarium ear mold (also referred to as Fusarium ear rot) is a devastating disease of maize caused by species of the Gibberella fuijkuroi complex, namely F. verticiffloides, F. proliferatum, and/or F. subglutinans. It is predominantly found in the southeastern United States, southern Europe, Mexico, Brazil, Argentina, and South Africa, and affects both grain yield and quality. Fusarium ear mold also results in contamination by several mycotoxins, including fumonisins (FUM), moniliformin (MON), and/or beauvericin, which appear to cause a number of human and animal diseases. Fumonisins, e.g., are linked to several animal toxicoses including leukoencephalomalacia (Marasas et al. (1988) Onderstepoort J. Vet. Res. 55:197-204; Wilson et al. (1990) American Association of Veterinary Laboratory Diagnosticians Abstracts 33rd Annual Meeting, Denver, Colo., Madison, Wis., USA) and porcine pulmonary edema (Colvin et al. (1992) Mycopathologia 117:79-82). Fumonisins are also suspected carcinogens (Geary et al. (1971) Coord. Chem. Rev. 7:81; Gelderblom et al. (1991) Carcinogenesis 12:1247-1251; Gelderblom et al. (1992) Carcinogenesis 13:433-437) and have been linked to birth defects in humans (Missmer et al. (2006) Environ Health perspect 114:237-41).
The etiology of Fusarium ear mold is poorly understood, although physical damage to the ear and certain environmental conditions can contribute to its occurrence (Nelson et al. (1992) Mycopathologia 117:29-36). When conditions for fungal growth are optimum, there are no cultural practices sufficient to minimize mycotoxin levels to a level deemed as “safe” by the Food and Drug Administration. Genetic resistance to Fusarium ear mold has been identified (Gendloff et al. (1986) Phytopathology 76:684-688; Holley et al. (1989) Plant Dis. 73:578-580), and several breeding efforts have led to the identification of maize germplasm with heritable resistance to Fusarium ear mold. However, incorporation of this resistance in maize inbred lines has been difficult. The use of phenotypic selection to introgress resistance is time consuming and difficult, and since Fusarium ear mold is sensitive to environmental conditions, selection for resistance from year to year based solely on phenotype has proven unreliable. In addition, specialized disease screening sites can be costly to operate, and plants must be grown to maturity in order to classify the level of resistance or susceptibility.
Selection through the use of molecular markers associated with is Fusarium ear mold resistance has the advantage of permitting at least some selection based solely on the genetic composition of the progeny. Moreover, resistance to Fusarium ear mold can be determined very early on in the plant life cycle, even as early as the seed stage. The increased rate of selection that can be obtained through the use of molecular markers associated with the Fusarium ear mold resistance trait means that plant breeding for Fusarium ear mold resistance can occur more rapidly, thereby generating commercially acceptable resistant plants in a relatively short amount of time. Thus, it is desirable to provide compositions and methods for identifying and selecting maize plants with enhanced resistance to Fusarium ear mold. These plants can be used in breeding programs to generate high-yielding hybrids with resistance to Fusarium ear mold.